The structure of Amiloride
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Amiloride

Amiloride is a potassium-sparing diuretic, first approved for use in 1967, used in the management of hypertension and congestive heart failure. more...

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Structure

Amiloride is a guanidinium group containing pyrazine derivative.

Mode of action

Amiloride works by inhibiting sodium reabsorption in the distal convoluted tubules and collecting ducts in the kidneys. This promotes the loss of sodium and water from the body, but without depleting potassium. The drug is often used in conjunction with thiazide or loop diuretics. Due to its potassium-sparing capacities, hyperkalemia (high blood potassium levels) are occasionally observed in patients taking amiloride. The risk is high in concurrent use of ACE inhibitors or spironolactone. Patients are also advised not to use potassium-containing salt replacements.

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Effect of dimethyl amiloride on chronic hypoxic pulmonary hypertension in rats - Thomas L. Petty 40th Annual Aspen Lung Conference: Biology & Pathobiology
From CHEST, 7/1/98 by Deborah Quinn

(CHEST 1998; 114:69S-70S)

The [Na.sup.+]/[H.sup.+] exchange regulation of intracellular pH may play a permissive role in pulmonary artery smooth muscle cell (PASMC) proliferation that occurs in hypoxia-induced pulmonary hypertension. Previously, this laboratory has demonstrated that dimethyl amiloride (DMA), an amiloride derivative with enhanced potency and selectivity as an inhibitor of the [Na.sup.+]/[H.sup.+] antiporter, can inhibit bovine PASMC proliferation stimulated by platelet-derived growth factor. In this study we studied whether DMA can inhibit hypoxic pulmonary hypertension in vivo as well. We hypothesized that DMA inhibits development of hypoxic pulmonary hypertension by interfering with PASMC growth. Sprague-Dawley rats were exposed to 10.5% [O.sub.2] for 14 days and were divided into three groups: hypoxia-DMA (n = 14, receiving DMA 3 mg/kg/day for 14 days intravenously through osmotic minipump), hypoxia-control (n=10), and normoxia-control (n=6). At the end of the DMA or saline treatment, hemodynamics, blood gas, and hematocrit were measured in anesthetized animals breathing room air to reverse any acute hypoxic vasoconstriction (Table 1).

(*) All data are shown are mean [+ or -] SE. Ppa=pulmonary-arterial pressure; CI=cardiac index; TPVRI=total pulmonary vascular resistance index (Ppa/CI); RV/LV+ S = right ventricle/left ventricle+septum; wall thickness refers to the terminal bronchiole; and thick vessels refers to intra-acinar vessels.

([dagger]) p<0.05, in comparison with normoxia-control group.

(double dagger]) p<0.05, in comparison with hypoxia-control group.

In conclusion, in spite of the hypertensive effects of polycythemia, DMA can significantly reduce pulmonary hypertension, fight ventricular hypertrophy, and vascular remodeling induced by chronic hypoxia.

(*) From the Pulmonary/Critical Care Unit Massachusetts General Hospital and Harvard Medical School, Boston. Supported by NIH Grant HL-39150.

COPYRIGHT 1998 American College of Chest Physicians
COPYRIGHT 2000 Gale Group

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